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This is a Cross-Sectional study.

September 10, 2025Open Access

Genetic damage and immune dysregulation in Schistosoma haematobium-infected individuals in Nigeria

Key Points

Infected individuals exhibited significant genetic damage markers, such as comet tail moment increased to 15.7 from 6.3 in controls.
Micronucleus frequency was markedly higher at 8.4 per 1000 cells in the infected group compared to 3.1 in controls, indicating severe genetic impact.
IL-4, IL-5, and IL-13 were elevated in infected individuals, reflecting the pronounced Th2 polarization in their immune response.
S. haematobium infection was identified as an independent predictor of genetic damage, explaining 73% of the variance in tail moment values.

Abstract

Urogenital schistosomiasis caused by Schistosoma haematobium affects over 100 million people globally, with potential long-term genetic and immunological consequences poorly understood in endemic populations. This study investigates genetic damage and immune dysregulation in infected individuals from a hyperendemic region in Nigeria. To quantify genetic damage markers and characterize immune system alterations in individuals with confirmed S. haematobium infection compared to uninfected controls from Atisbo Local Government Area, Oyo State, Nigeria. This cross-sectional study included 240 participants (120 infected, 120 controls) aged 15–65 years, selected using multi-stage cluster sampling. Genetic damage was assessed using comet assay, micronucleus testing, and chromosomal aberration analysis. Immune profiling included Th1/Th2 cytokines, immunoglobulins, and complement components. Multivariate regression models identified independent predictors of genetic damage. Infected individuals demonstrated markedly elevated genetic damage: comet tail moment 15.7 ± 4.2 versus 6.3 ± 2.1 (Cohen's d = 2.80, p < 0.001), micronucleus frequency 8.4 ± 2.7 versus 3.1 ± 1.2 per 1000 cells (d = 2.41, p < 0.001), and chromosomal abnormalities 12.3% versus 4.1% (p < 0.001). Pronounced Th2 polarization was evident with IL-4 increased 4.1-fold, IL-5 4.6-fold, and IL-13 4.1-fold, while IFN-γ was reduced by 65% (all p < 0.001, FDR-adjusted). S. haematobium infection independently predicted genetic damage (β = 8.42, 95% CI: 7.51–9.33, p < 0.001) after adjusting for age, BMI, hemoglobin, and sex, explaining 73% of the variance in tail moment values. S. haematobium infection causes substantial genetic damage and Th2-dominant immune dysregulation with potentially serious long-term health consequences. These findings provide scientific justification for intensified control efforts, enhanced post-treatment monitoring, and cancer surveillance programs in endemic populations.

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